tbuckley/cabot-search huggingface dataset:
Skin Pigmentation and Acute Renal Failure in a Patient Receiving Phenazopyridine Therapy
Authors: Carl E. Eybel
Journal: JAMA (1974)

ACUTE renal failure and skin pigmentation secondary to phenazopyridine hydrochloride therapy have been previously described in patients with preexisting renal dysfunction.<sup>1</sup>The present report concerns a patient with apparently reasonable prior renal function who, while receiving usual doses of the phenazopyridine, developed yellowish-orange pigmentation of the skin and of urinary casts, and acute renal insufficiency. <h3>Report of a Case</h3> An 85-year-old white woman was admitted to the hospital in December 1970 because of atrial fibrillation, angina pectoris, and left ventricular failure. Her medications included pentaerythritol tetranitrate and sublingual nitroglycerine (Nitrol tablets). On physical examination, apart from her cardiopulmonary manifestations, she was also found to have suprapubic and bilateral costovertebral angle tenderness. Laboratory determinations included the following: hemogram, serum electrolytes, bilirubin, protein electrophoresis, glutamic oxaloacetic and glutamic pyruvic transaminases, alkaline phosphatase, and protein-bound iodine. All were within normal limits. Serum urea nitrogen and creatinine values were 10 mg/100 ml and
Editorial: Control of spasticity.
Authors: Charles Dodds
Journal: BMJ (1973)

found whose mother did not have the anomaly.On these findings it would seem that some familial factor does contribute to the production of multiple sclerosis and that it operates more strongly through females than through males.Clearly further work is required in the development of this particular thesis, and it may be that these initial findings will prove to be less solid than they seem.Yet this demonstration of the possible familial and environmental implications is impressive.
Toxicology. The Nature, Effects and Detection of Poisons, with the Diagnosis and Treatment of Poisoning.
Journal: JAMA (1902)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Ganglioside Changes Induced by Tumor Promoters in Promotable JB6 Mouse Epidermal Cells: Antagonism by an Antipromoter
Journal: JNCI Journal of the National Cancer Institute (1982)

Since cell surface gangliosides have been implicated in the regulation of cell growth and differentiation and since tumor-promoting phorbol esters produce a number of membrane changes. the possibility was investigated that ganglioside changes may playa role in promotion of transformation in JB6 mouse epidermal cells. The studies showed that tumor-promoting but not non-promoting phorbol esters produced decreased precursor incorporation into trisialogan-glioside GT and increased incorporation into disialoganglioside GD1b and an unknown ganglioside. GX. These ganglioside responses to promoters were antagonized by the antipromoter retinoic acid. thus suggesting that alterations in ganglioside levels may be involved in promotion of transformation.
Malignant atrophic papulosis
Authors: R. Degos
Journal: British Journal of Dermatology (1979)

Journal Article Malignant atrophic papulosis Get access R. Degos R. Degos Pavillion Gougerot, Hôpital St Louis, 2 Place Alfred Fournier, 75010 Paris, France Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 101, Issue 6, 1 December 1979, Page 734, https://doi.org/10.1111/j.1365-2133.1979.tb05660.x Published: 01 December 1979
Implantation of an Artificial Pancreas
Authors: David S. Schade
Journal: JAMA (1981)

DURING the 1970s, implantation of an artificial pancreas as a potential cure for diabetes received much publicity. Recently, successful diabetic treatment with explanted insulin delivery devices<sup>1</sup>has accelerated efforts toward total implantation. Despite this enthusiasm, the clinical timetable for implantation in diabetic humans is unresolved. Both our group and others have successfully implanted dogs with insulin delivery systems for periods ranging from weeks to months.<sup>2,3</sup>Advances in technology of insulin delivery systems have been so rapid that within months, remotely controlled implantable insulin delivery devices will be available to many investigators, including ourselves. With more than 5 million diabetic patients in this country, should widespread, clinical implantation of these devices begin immediately? The answer to this question relates to the benefits vs the risks of implantation. Loss of endocrine pancreatic function (ie, insulin secretion) does not result in death, as occurs with the loss of kidney or cardiac function.
Highlights of This Issue
Journal: Clinical Cancer Research (2010)

Angiogenesis plays a crucial role in the development of bone metastases. To examine vascular changes in experimental breast cancer bone metastases upon treatment with zoledronic acid and sunitinib malate, Bäuerle and colleagues used dynamic contrast enhanced MRI and vessel size imaging in a longitudinal in vivo study. Resulting parameters from noninvasive imaging indicated vessel remodeling in these osseous lesions after application of zoledronic acid and sunitinib malate, which could be assessed before antiresorptive and antitumor effects of these treatments were detected. These results suggest that imaging could be used for early assessment of treatment response in malignant bone lesions.In recent years, the study of cancer stem cells (CSCs) has garnered much attention. In this issue of CCR Focus, guest editor Percy Ivy provides an overview of research surrounding CSCs and addresses some of the controversies in the field. Topics in CSC biology are discussed, including CSC identification and characterization, the CSC self-renewal pathway, and interaction of CSCs with the microenvironment. A particular emphasis is placed on translating our underlying knowledge of CSC biology into the development of anticancer therapeutics, and efforts to target several pathways involved in CSCs, including the Wnt, Notch, and Hedgehog signaling pathways, are described.Histone deacetylases (HDACs) 1–11 are differentially expressed in cancer tissues; however, more research is needed on the role of individual HDACs in tumor biology. In this study, Milde and colleagues found that class II HDACs 5 and 9 were significantly upregulated in medulloblastoma tumors with poor prognosis, and high HDAC5 and HDAC9 mRNA expression was an independent risk factor for poor survival in multifactorial analysis. Furthermore, siRNA-mediated knockdown of HDAC5 or HDAC9 resulted in decreased tumor cell growth. These findings implicate HDAC5 and HDAC9 as potential therapeutic targets in medulloblastoma.Local CD40-directed therapies, which aim to tilt tumor-induced immunosuppression in favor of antitumor responses, have shown promise in experimental models. Malmström and colleagues used adenovector-based gene therapy to introduce the human CD40 ligand (CD40L) gene into the tumor milieu. In a Phase I/IIa trial of patients with urinary bladder carcinoma, they found that AdCD40L therapy was safe and that it stimulated a massive immune cell infiltration into the bladder wall. Further, several patients had few, or no, remaining high-grade malignant cells following treatment. These results suggest that AdCD40L therapy has potential for local application on patients with solid tumors.
High Blood Pressure: Its Variations and Control. A Manual for Practitioners.
Journal: JAMA (1927)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Abstract 34: STIM1 Increases Calcium Stores in the Sarcoplasmic Reticulum of Adult Feline Ventricular Myocytes
Authors: Constantine Troupes, Sadia Mohsin, Remus Berretta, Hajime Kubo, Jonathan Soboloff, Steven Houser
Journal: Circulation Research (2015)

Background: STIM1 is a Sarcoplasmic Reticulum (SR) membrane resident protein implicated in sensing and maintaining SR Ca2+ levels. The role of STIM1 in the regulation of SR Ca2+ stores in the normal and diseased heart is not well described. Previous reports confirm that STIM1 is present at low levels in the healthy adult heart, but expression levels increase after cardiac injury. Objective: To determine if increased STIM1 expression after cardiac injury may be involved in the disturbed Ca2+ cycling present within diseased cardiomyocytes. Results: We used adenovirus to express either STIM1 or red fluorescent protein (RFP) in freshly isolated adult feline ventricular myocytes (AFMs). After 48 hours in culture, STIM1 induced cell death in 60% of myocytes versus only 5% in RFP controls. Addition of nifedipine rescued the cell death caused by STIM1, but block of transient receptor potential canonical (TRPC) channels was unable to improve viability. AFMs expressing STIM1 exhibited increased fractional shortening and Ca2+ transient amplitude, which was associated with increased SR load. Interestingly, high SR load levels caused by STIM1 were not reduced by nifedipine addition. We also found that baseline L-type channel current amplitude was significantly reduced by 20%, but no difference in current amplitude was found after Bay K8644 addition. Conclusions: In this study, we found that STIM1 caused Ca2+ overload leading to cell death. This process was L-type channel dependent, but TRPC channels were not involved. STIM1 also caused increased SR load at rest, which was not altered by nifedipine revealing that STIM1 mediated Ca2+ influx does not require L-type channel activity but Ca2+ influx through L-type channels is essential for STIM1 induced cellular death. Furthermore, STIM1 reduced L-type current activity but did not alter channel availability. These data show that after cardiac injury, STIM1 is likely to play a role in regulating cell survival as well as excitation-contraction coupling.
Laboratory Profile Screening in the Family Physician's Office
Authors: Thomas E. Rardin
Journal: JAMA (1966)

An increase in the use of routine automated laboratory profile screening, included as an essential part of each annual health evaluation, has been predicted and urged by various authorities. Three recent studies indicate 10% of those screened will show some major chemical abnormality. One key specialist in the evaluation of any person's health status is his family physician. This report considers data from a fourth study, consisting of 1,084 consecutive automated laboratory profiles secured on 832 adult patients having health evaluations performed by their family physician. Both patient and physician benefit greatly. The suggestion by many authorities that the apparently healthy person as well as the obviously sick patient be routinely studied by automated laboratory profile screening seems justified.
The Patient as a "Whole Man"
Authors: M. A. Casberg
Journal: JAMA (1967)

There has been a great deal of recent publicity in both the lay press and in scientific periodicals about the changing patterns of the practice of medicine. The medical profession has been accused of being "impersonal" and it is a current fad to denounce the physician for "not taking a more personal interest in the patient." Many of these criticisms emanate from biased sources, of course, and not infrequently the critic is unaware of the fundamental changes in diagnosis and therapy. I would appreciate comments from your consultants in the form of a candid discussion of what the physician's concept of his professional obligations to his patients should be. Have the salutary effects of medical progress been accompanied by an unfortunate erosion of the personal identity of the patient? What do we mean by the consideration of the patient as a whole man?
The Problem-Oriented Record
Authors: Mark D. Aronson
Journal: JAMA (1973)

A two-column modification of the problem-oriented record is presented that (1) provides one way to reduce the large amount of data collected on an average hospitalized patient, (2) can function as an effective teaching and auditing tool by providing immediate feedback to the intern or student on his workup, (3) can reduce the time outlay of residents by eliminating the need to repeat written histories and physicals, and (4) can serve as a tool to more carefully audit a resident's contributions, satisfying the recent requirements of the Board of Internal Medicine.
Brain Serotonin Neurotoxicity and Primary Pulmonary Hypertension From Fenfluramine and Dexfenfluramine
Authors: Una D. McCann
Journal: JAMA (1997)

<h3>Objectives.</h3> —Obesity is an important clinical problem, and the use of dexfenfluramine hydrochloride for weight reduction has been widely publicized since its approval by the Food and Drug Administration. However, animal and human studies have demonstrated toxic effects of fenfluramines that clinicians should be aware of when considering prescribing the drugs. Our purpose was to systematically review data on brain serotonin neurotoxicity in animals treated with fenfluramines and the evidence linking fenfluramines to primary pulmonary hypertension (PPH). <h3>Data Sources.</h3> —Archival articles and reviews identified through a computerized search of MEDLINE from 1966 to April 1997 using "fenfluramine(s)," "serotonin," "neurotoxicity," "behavior," "anorexigens," "weight loss," and "primary pulmonary hypertension" as index terms. <h3>Study Selection.</h3> —Reports dealing with long-term effects of fenfluramines on brain serotonin neurons, body weight, and pulmonary function in animals and humans. <h3>Data Extraction.</h3> —Reports were reviewed by individuals with expertise in serotonin neurobiology, neurotoxicity, neuropsychiatry, and pulmonary medicine and evaluated for appropriateness for inclusion in this review. <h3>Data Synthesis.</h3> —Fenfluramines cause dose-related, long-lasting reductions in serotonin axonal markers in all the animal species tested and with all the routes of drug administration used. Doses of fenfluramines that produce signs of brain serotonin neurotoxicity in animals are on the same order as those used to treat humans for weight loss when one takes into account known relations between body mass and drug clearance. However, no human studies have been conducted, and the pathological and clinical potential for neurotoxicity in humans is unknown. Appetite suppressants—most commonly fenfluramines—increase the risk of developing PPH (odds ratio, 6.3), particularly when used for more than 3 months (odds ratio, &gt;20). <h3>Conclusions.</h3> —Fenfluramine and dexfenfluramine have been demonstrated to damage brain serotonin neurons in animal studies. It is not known if such damage occurs in humans or if there are clinical consequences. Use of fenfluramines is associated with an increased risk of PPH. Future studies should address the long-term consequences of prolonged use of fenfluramines.
Resources for Coronary Artery Surgery
Authors: Irving S. Wright
Journal: JAMA (1972)

Aortocoronary vein bypass is the most recent and promising of the surgical procedures for revascularizing the heart. At present there is a wide range of opinion regarding indications for this operation and the environment in which it should be carried out. Many physicians now feel under pressure to recommend the procedure for increasing numbers of patients and this in turn has resulted in pressure on hospitals for new and expanded cardiac surgical programs. Therefore, the time is right for an authoritative statement on the current status of this operation with guidelines for establishing quality surgical programs for these patients. The recent statement of the Inter-Society Commission for Heart Disease Resources (ICHD)<sup>1</sup>does much to fill this need. The ICHD was created three years ago under a grant from the Regional Medical Programs Service to develop guidelines for optimal medical resources for the prevention and care of patients with cardiovascular
Hospital emergency room liability cases
Journal: JAMA (1969)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Highlights from Recent Cancer Literature
Journal: Cancer Research (2017)

Precision Treatment for GlioblastomaTo better delineate relationships between heterogeneity and treatment response in glioblastoma, Lee and colleagues sequenced DNA and RNA from multiple biopsies across individual patients.Whereas IDH1 mutations, PIK3CA mutations, and FGFR3-TACC3 fusions were generally clonal, PTEN alterations and EGFR amplification/mutation were not.Calculating genetic distances among multisector samples, they found multiple tumors from distant regions and long-term recurrences had greater diversity compared with locally adjacent tissues.Single cell transcriptomics revealed individual cells harbored distinct EGFR alterations, whereas PIK3CA mutations were present in all cells.In 28 patient-derived cells from 11 individuals, genetic distance correlated with drug response.Distant and longitudinal samples showed broader drug responses than local samples, specifically a higher sensitivity to PI3K-AKT-mTOR inhibition.Not surprisingly, multisector patient-derived cells were more sensitive to drugs targeting shared events, suggesting a need to target truncal events in glioblastoma.(Image by John Dalton courtesy of
Морфофункціональні зміни печінки щурів з експериментальним гепатитом в умовах дисбалансу оксиду азоту
Authors: V.I. Didenko, I.A. Klenina, A.I. Rudenko, V.A. Makarchuk, N.Yu. Oshmianska, O.O. Halinskyi
Journal: GASTROENTEROLOGY (2014)

Встановлено, що через 7 днів після чотириразового введення чотирихлористого вуглецю (ССl4) в печінці щурів розвивається гострий гепатит, основою якого є переважно поширена жирова дистрофія, яка займає 40–80 % всієї площі біоптату та завжди локалізована навколо портальних трактів з найбільшим ураженням І–ІІ зони ацинусів. Морфологічні зміни в І групі супроводжувалися підвищенням активності аргінази (АР) в гомогенатах печінки щурів на 50,0 % (р &lt; 0,01), а вміст метаболітів оксиду азоту (NОх) був зниженим на 20,0 % (р &lt; 0,01) порівняно з контрольною групою. Також спостерігалося зниження кількості відвідуваних щурами зовнішніх квадратів на 79,4 %, а внутрішніх — на 78,3 % порівняно з конт-рольною групою (р &lt; 0,001). Через 7 днів після одноразового введення ССl4 (ІІ група) вiдмічалася схожа з І групою морфологічна картина, але у ряді випадків зміни характеризувалися меншою інтенсивністю. Розвиток експериментального гепатиту на тлі нестачі оксиду азоту в 100 % випадків характеризувався вираженим розширенням синусоїдів по всій площині біоптату. Руйнування гепатоцитів внаслiдок жирової дистрофії мало більш локальний характер. У щурів ІІІ групи відбувалося інгібування активності АР на 22,1 % (р &lt; 0,05) та зниження вмісту NОх на 21,5 % порівняно з контрольною групою.Розвиток гострого гепатиту на тлі надлишку оксиду азоту у 75,0 % тварин супроводжувався менш поширеною, але більш вираженою жировою дистрофією з локальними фокусами некрозу. Активність АР мала тенденцію до підвищення на 9,9 % порівняно з контрольною групою, виявлена тенденція до зниження NОх на 16,1 %, що аналогічно біохімічним показникам І групи. Тварини групи одноразового введення CCl4 на тлі 5-добового надлишку NO характеризувалися зниженою руховою і орієнтовно-дослідницькою активністю. Отримані дані свідчать про те, що нами відтворена модель гепатиту шляхом однарозового введення CCl4 на тлі надлишку NO. Це підтверджувалося характерними для гепатиту морфологічними змінами та компенсаторною відповіддю організму у вигляді підвищення активності аргінази та зменшенням вмісту метаболітів оксиду азоту в гомогенаті печінки. Одноразове введення CCl4 на фоні надлишку NO призводило до порушення як рухової активності, так і орієнтовно-дослідницької діяльності піддослідних тварин.
Endoscopy International Open – recently published
Journal: Endoscopy (2017)

Comment on: First clinical experiences with a novel endoscopic over-the-scope clip system Endosc Int Open 2017; 05(03): E151-E156DOI: 10.1055/s-0043-101692 Comment on: First reported case of per anal endoscopic myectomy (PAEM): A novel endoscopic technique for resection of lesions with severe fibrosis in the rectumEndosc Int Open 2017; 05(03): E146-E150DOI: 10.1055/s-0042-122965 Comment on: Safety and efficacy of minimal biliary sphincterotomy with papillary balloon dilation (m-EBS+EPBD) in patients using clopidogrel or anticoagulation Endosc Int Open 2017; 05(03): E157-E164DOI: 10.1055/s-0042-120225